Relationship between sex hormones, body composition and metabolic risk parameters in premenopausal women

1995 ◽  
Vol 133 (2) ◽  
pp. 200-206 ◽  
Author(s):  
Steen B Pedersen ◽  
Jens D Børglum ◽  
Kim Brixen ◽  
Bjørn Richelsen

Pedersen SB, Borglum JD, Brixen K, Richelsen B. Relationship between sex hormones, body composition and metabolic risk parameters in premenopausal women. Eur J Endocrinol 1995;133: 200–6. ISSN 0804–4643 The metabolic complications associated with obesity are dependent upon the degree of obesity and the distribution of adipose tissue. In order to evaluate the associations between sex hormone status, metabolic risk parameters, obesity and distribution of adipose tissue, 25 premenopausal women with a wide range of body mass index (19.3–48.1 kg/m2 were studied. Body composition was determined by dual-energy x-ray absorptiometry scan and anthropometric measurements; in addition, lipid and sex hormone status were determined and an oral glucose tolerance test was performed. We found that sex hormone-binding globulin was correlated negatively with total fat mass (r = –0.77, p < 0.001) and especially with abdominal localization of adipose tissue (r = –0.85, p < 0.001). Free testosterone was correlated positively with total fat mass (r = 0.40, p < 0.05) and with abdominal fat accumulation (r = 0.64, p < 0.001). Free estrogen was correlated negatively with total amount of adipose tissue (r = –0.40, p < 0.05) but not with the distribution of adipose tissue, Finally, total fatness, abdominal localization of adipose tissue and free testosterone were all associated with elevated metabolic risk factors. However, multiple regression analysis revealed that only abdominal localization of adipose tissue was independently associated with a higher risk profile, whereas the effects of sex hormones or total fatness disappeared when abdominal localization of adipose tissue was included in the analysis. In conclusion, these findings in premenopausal women indicate that the connection between sex hormones and metabolic risk factors might be indirect, probably operating through alterations in the amount of adipose tissue in the abdominal region. SB Pedersen, University Clinic of Endocrinology and Internal Medicine, Aarthus, Amtssygehus, Tage Hansensgade, DK-8000 Aarhus C, Denmark

Gene ◽  
2018 ◽  
Vol 646 ◽  
pp. 74-82 ◽  
Author(s):  
Yuchang Yao ◽  
Hongying Ma ◽  
Keliang Wu ◽  
Yonggang Shao ◽  
Wenpeng Han ◽  
...  

2014 ◽  
Vol 23 (12) ◽  
pp. 2943-2953 ◽  
Author(s):  
Kelly A. Hirko ◽  
Donna Spiegelman ◽  
Walter C. Willett ◽  
Susan E. Hankinson ◽  
A. Heather Eliassen

2017 ◽  
Vol 42 (8) ◽  
pp. 921-923 ◽  
Author(s):  
C. Bernárdez ◽  
A. M. Molina-Ruiz ◽  
S. Vañó-Galvan ◽  
M. Urech ◽  
D. Saceda-Corralo ◽  
...  

2000 ◽  
Vol 85 (1) ◽  
pp. 35-41
Author(s):  
Colleen Hadigan ◽  
Colleen Corcoran ◽  
Takara Stanley ◽  
Sarah Piecuch ◽  
Anne Klibanski ◽  
...  

Fat redistribution in the setting of protease inhibitor use is increasingly common and is associated with insulin resistance in human immunodeficiency virus (HIV)-infected patients. However, little is known regarding the factors that may contribute to abnormal insulin regulation in this population. We assessed fasting insulin levels in HIV-infected men and determined the relationship among insulin, body composition, endogenous gonadal steroid concentrations, and antiviral therapy in this population. We also determined the effects of exogenous testosterone administration using the homeostatic model for insulin resistance (HOMA IR) in hypogonadal HIV-infected men with the acquired immunodeficiency syndrome wasting syndrome. Fifty HIV-infected men with acquired immunodeficiency syndrome wasting were compared with 20 age- and body mass index (BMI)-matched healthy control subjects. Insulin concentrations were significantly increased in HIV-infected patients compared to those in control patients (16.6 ± 1.8 vs. 10.4 ± 0.8 μU/mL; P &lt; 0.05) and were increased in nucleoside reverse transcriptase (NRTI)-treated patients who did not receive a protease inhibitor (PI; 21.7 ± 4.3 vs. 10.4 ± 0.8μ U/mL; P &lt; 0.05). Insulin concentrations and HOMA IR were inversely correlated with the serum free testosterone concentration (r = −0.36; P = 0.01 for insulin level; r = −0.30; P = 0.03 for HOMA), but not to body composition parameters, age, or BMI. In a multivariate regression analysis, free testosterone (P = 0.05), BMI (P &lt; 0.01), and lean body mass (P = 0.04) were significant. Lower lean body mass and higher BMI predicted increased insulin resistance. The HIV-infected patients demonstrated an increased trunk fat to total fat ratio (0.49 ± 0.02 vs. 0.45 ± 0.02; P &lt; 0.05) and an increased trunk fat to extremity fat ratio (1.27 ± 0.09 vs. 0.95 ± 0.06, P = 0.01), but a reduced extremity fat to total fat ratio (0.44 ± 0.01 vs. 0.49 ± 0.01; P = 0.02) and reduced overall total body fat (13.8 ± 0.7 vs. 17.2 ± 0.9 kg; P &lt; 0.01) compared to the control subjects. Increased truncal fat and reduced extremity fat were seen among NRTI-treated patients, but this pattern was most severe among patients receiving combined NRTI and PI therapy [trunk fat to extremity ratio, 1.47 ± 0.15 vs. 0.95 ± 0.06 (P &lt; 0.01); extremity fat to total fat ratio, 0.40 ± 0.02 vs. 0.49 ± 0.01 (P &lt; 0.05)]. Insulin responses to testosterone administration were investigated among 52 HIV-infected men with hypogonadism and wasting (weight &lt;90% ideal body weight and/or weight loss &gt;10%) randomized to either testosterone (300 mg, im, every 3 weeks) or placebo for 6 months. Testosterone administration reduced HOMA IR in the HIV-infected men (−0.6 ± 0.7 vs. +1.41 ± 0.8, testosterone vs. placebo, P = 0.05) in association with increased lean body mass (P = 0.02). These data demonstrate significant hyperinsulinemia in HIV-infected patients, which can occur in the absence of PI use. In NRTI-treated patients not receiving PI, a precursor phenotype is apparent, with increased truncal fat, reduced extremity fat, and increased insulin concentrations. This phenotype is exaggerated in patients receiving PI therapy, with further increased truncal fat and reduced extremity fat, although hyperinsulinemia per se is not worse. Endogenous gonadal steroid levels are inversely related to hyperinsulinemia in HIV-infected men, but reduced lean body mass and increased weight are the primary independent predictors of hyperinsulinemia. Indexes of insulin sensitivity improve in response to physiological androgen administration among hypogonadal HIV-infected patients, and this change is again related primarily to increased lean body mass in response to testosterone administration.


Diabetes Care ◽  
1999 ◽  
Vol 22 (9) ◽  
pp. 1471-1478 ◽  
Author(s):  
A. Pascot ◽  
S. Lemieux ◽  
I. Lemieux ◽  
D. Prud'homme ◽  
A. Tremblay ◽  
...  

2013 ◽  
Vol 10 (5) ◽  
pp. 727-733 ◽  
Author(s):  
Lauren E. Gyllenhammer ◽  
Amanda K. Vanni ◽  
Courtney E. Byrd-Williams ◽  
Marc Kalan ◽  
Leslie Bernstein ◽  
...  

Background:Lifetime physical activity (PA) is associated with decreased breast cancer (BC) risk; reports suggest that PA during adolescence contributes strongly to this relationship. PA lowers production of sex hormones, specifically estradiol, or decreases insulin resistance (IR), thereby lowering risk. Overweight Latina adolescents are insulin resistant and exhibit low levels of PA, potentially increasing their future BC risk.Methods:37 obese Latina adolescents (15.7 ± 1.1 yrs) provided measures of PA using accelerometry; plasma follicular phase estradiol, sex-hormone binding globulin, total and free testosterone, dehydroepiandrosterone-sulfate (DHEAS); IR using HOMA-IR; and body composition via DEXA. Partial correlations and stepwise linear regressions assessed cross-sectional relationships between sex hormones, IR and PA. Body composition, and age were included a priori as covariates.Results:Estradiol was negatively associated with accelerometer counts per minute (CPM; r = −0.4; P = .02), percent time spent in moderate PA (%MPA; r = −0.5; P = .006), and percent time in moderate or vigorous PA (%MVPA; r = −0.5; P = .007). DHEAS was positively associated with CPM (r = .4, P = .009), %MPA (r = .3, P = .04), and %MVPA (r = .3, P = .04). Other sex hormones and IR were not associated with PA measures.Conclusion:This study is the first to show that higher habitual PA was inversely associated with estradiol in obese adolescents.


2019 ◽  
Vol 104 (9) ◽  
pp. 4119-4126
Author(s):  
Oscar Bergens ◽  
Andreas Nilsson ◽  
Fawzi Kadi

Abstract Context Chronic inflammation increases diabetes risk and may be exacerbated by excess adipose tissue. Whether cardiovascular fitness can offset chronic inflammation associated with excess adipose tissue in older adults is unclear. Objective The study aimed to examine the influence of cardiorespiratory fitness on links between adiposity and pro- and anti-inflammatory biomarkers related to metabolic risk in physically active older women. Design, Setting, and Participants Cross-sectional study comprising older community-dwelling women (n = 109; age, 65 to 70 years). Main Outcome Cardiorespiratory fitness was assessed using a standardized submaximal test and participants were categorized into high- and low-adiposity–related metabolic risk [body mass index, waist-to-hip ratio (WHR), and total fat mass]. The inflammatory biomarkers C-reactive protein (CRP), IL-6, IL-10, IL-18, adiponectin, monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein (MIP)-1α were analyzed. Results Regardless of adiposity measure, women in the metabolic high-risk group had substantially elevated (P < 0.05) CRP and lower adiponectin levels. Levels of IL-6 and MIP1-α were elevated in the high-risk group defined by WHR and total fat mass. The IL-18 level was elevated in the high-risk group based on WHR only. Importantly, a high cardiorespiratory fitness level did not attenuate the detrimental links between adiposity measures and inflammation. Conclusions Cardiorespiratory fitness does not offset the detrimental links between adiposity and several inflammatory biomarkers related to metabolic risk in physically active older women. Reducing abdominal adipose tissue in older adults should be emphasized in efforts aiming to attenuate age-related systemic inflammation and metabolic risk regardless of cardiorespiratory fitness.


2021 ◽  
pp. 1-10
Author(s):  
Ya-Wen Chen ◽  
Dong Hang ◽  
Ane S. Kværner ◽  
Edward Giovannucci ◽  
Mingyang Song

Abstract The objective was to investigate associations between life-course adiposity and sex hormone concentrations: trajectory of adiposity from age 5 to 40 (premenopausal)/60 (postmenopausal women and men) in relation to levels of oestrone (E1), oestradiol (E2), sex hormone-binding globulins (SHBG), testosterone in 4801 premenopausal and 6019 postmenopausal women in the Nurses’ Health Study (NHS) and NHS II, and 2431 men in the Health Professionals Follow-up Study. We used group-based trajectory models to identify groups within each cohort based on recalled somatotypes and reported BMI. Multivariate linear regression models were used to compare sex hormone concentration across different trajectory groups. The mean age at blood draw was 64·1 ± 8·1 years for men, 59·4 ± 6·0 for postmenopausal and 44·1 ± 4·6 for premenopausal women. In men, compared with the medium-stable group, lean-marked increase and medium increase groups had lower levels of SHBG (percentage difference: −17 and −9 %) and testosterone (−15 and −13 %). In postmenopausal women, compared with the medium-stable group, lean-marked increase and medium increase groups had higher levels of E1 (21 and 34 %) and E2 (45 and 68 %) but lower level of SHBG (–29 and −35 %). In premenopausal women, compared with the lean-moderate increase group, medium-stable/increase and heavy-stable/increase groups had lower levels of SHBG (–6 and −28 %). Attained adulthood adiposity and middle-life weight gain were associated with lower SHBG and testosterone in men, higher E1 and E2 and lower SHBG in postmenopausal women, and lower SHBG in premenopausal women. The study indicates the importance of maintaining a healthy body weight throughout life course for homoeostasis of sex hormones.


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